Adhesion and clustering of charge isomers of myelin basic protein at model myelin membranes

The association of myelin basic protein charge isomers with the lipid part of the myelin membrane was investigated at the microscopic (molecular) level in a model membrane system, using optical waveguide lightmode spectrometry to determine with high precision the kinetics of association and dissociation to planar phospholipid membranes under controlled hydrodynamic conditions and over a range of protein concentrations. Detailed analysis of the data revealed a rich and intricate behaviour and clearly showed that the membrane protein affinity is characterized by at least four independent parameters: (i) the association rate coefficient characterizing the protein-membrane interaction energy as the protein approaches the fluid-membrane interface; (ii) the protein-membrane adhesion, i.e., the probability that it will remain at the membrane after arrival; (iii) the protein conformation at the membrane; and (iv) the protein's tendency to cluster at the membrane. Some of these parameters varied in characteristic ways as the bulk solution concentration of the protein was varied, giving further clues to the detailed molecular comportment of the protein. The parameters and their characteristic variations with bulk concentration were markedly different for the different isomers. Implications of these results for neurological disorders involving demyelination, such as multiple sclerosis, are discussed.     

Experimental informational neuroses in dogs as sequelae of overloading short-term memory

In conditions of overloaded function of short-term memory, studied by the method of delayed reactions, with a prolonged deficit of time allotted for realization of the function, the animals exhibit substantial disturbances of higher nervous activity which by their etiological character belong to the group of informational neuroses. Appearance of the neurosis is preceded by a number of complex behavioral and vegetative changes reflecting activation of powerful compensatory mechanisms of the brain activity, aimed at elimating the time deficit and other neurotizing factors of the surroundings. Experimental neurosis caused by overloading the function of short-term memory is characterized by a severe course and is attended with motor and somatic disturbances as well as by memory and emotional disorders.